RT Journal Article SR Electronic T1 T cell responses to a non-glycosylated epitope predominate in type II collagen-immunised HLA-DRB1*0101 transgenic mice JF Annals of the Rheumatic Diseases JO Ann Rheum Dis FD BMJ Publishing Group Ltd and European League Against Rheumatism SP 599 OP 604 DO 10.1136/ard.2006.061945 VO 66 IS 5 A1 Alexei von Delwig A1 Daniel M Altmann A1 Fraser G Charlton A1 Norman McKie A1 John D Isaacs A1 Rikard Holmdahl A1 John H Robinson YR 2007 UL http://ard.bmj.com/content/66/5/599.abstract AB Aim: To study collagen-induced arthritis in human leucocyte antigen (HLA)-DR1 transgenic mice lacking endogenous major histocompatibility complex class II molecules (MHC-II) and to determine T cell specificity against the arthritogenic CII259–273 epitope of type II collagen either unmodified or post-translationally glycosylated at Lys264.Methods: Arthritis was induced by immunisation with human type II collagen in complete Freund’s adjuvant and measured by footpad swelling, clinical score and histology. T cell responses were assessed by proliferation of spleen and lymph node cells and in antigen presentation assays, using T cell hybridomas specific for the glycosylated and non-glycosylated CII259–273 epitope.Results: The incidence of arthritis was 50% in DR1-transgenic mice lacking endogenous MHC-II molecules. Recall T cell responses in draining lymph nodes and spleen were consistently greater against the non-glycosylated epitope than to the glycosylated CII259–273. Most of the T cell hybridomas generated from CII-immunised mice recognised the non-glycosylated CII epitope and this form of the epitope was also presented with 100-fold higher efficiency and 1 h faster kinetics by both macrophages and dendritic cells.Conclusion: This study shows that T cell responses to the non-glycosylated epitope of heterologous (human) CII are dominant in HLA-DR1 transgenic mice lacking MHC-II, which could contribute to the pathogenicity of autoimmune arthritis.